TCAs

[asecin]

so since i was a way for a while, how come nobody on this forum reported any experience with TCAs ? originally that what i had in mind. to create this thread in a way to encourage people on this forum who have been using those type of antidepressants and to come and share their experiences. yet, most of the replies are just general speculations of some of the descriptions you have been reading off wikipedia.

 

[sekio]

so since i was a way for a while, how come nobody on this forum reported any experience with TCAs ?

You never asked. It would be best to ask questions of that sort on Other Drugs though - that forum gets a lot more traffic and ADD is more for discussions of the mechanisms behind how drugs work rather than subjective experience reports of common psychotropics.

 

[pizzystrizzy]

so since i was a way for a while, how come nobody on this forum reported any experience with TCAs ? originally that what i had in mind. to create this thread in a way to encourage people on this forum who have been using those type of antidepressants and to come and share their experiences. yet, most of the replies are just general speculations of some of the descriptions you have been reading off wikipedia.

I've taken several -- imipramine, for a month; Amitriptyline, a couple times to sleep; & desipramine, for about a year (before switching to bupropion xl). I've also taken mirtazapine. What I've posted above was consistent with my experiences. (Also I've contributed significantly to several wikipedia articles on many of these drugs and am active w/ wikiprojectharmacology)

 

[arctica]

I took imipramine for a year or so. It worked OK for a while, and then pooped out. The dry mouth thing was a little annoying, but the side effects were mild compared to some of the other psych drugs I've been on (I'm looking at you, Viibryd and Cymbalta and lithium) I found the most annoying thing to be the drug interactions. The other reason that TCAs have fallen out of favor is that many of the newer drugs aren't contraindicated with everything under the sun. You can forget about taking just about any OTC cold medication, Sudafed, etc.

http://www.drugs.com/drug-interactions/imipramine-index.html?filter=3&generic_only=

One of my friends was recently diagnosed with cardiac damage, which her doctors are attributing to Elavil/amitryptyline. I think it's a problem which is more often seen in elderly patients, but apparently it happens in younger patients too, so it's something to watch for.

According to my shrink and people who have been put on MAOIs more recently, the risk of hypertensive crisis as a result of eating the wrong thing has been totally overblown, even for the old school MAOIs like Nardil. I was told you have to watch what you eat to a certain extent, but if you don't have pre-existing conditions like hypertension, you can eat reasonable portions of the "forbidden" foods. If you eat too much, you don't feel so hot and get a ripping headache, and then you don't eat whatever it was you ate again, at least in that quantity. You are unlikely to keel over or stroke out from having a glass of wine, but of course, YMMV.

This is my own pet theory, but I think that part of the renewed interest in older antidepressants is because TCAs and MAOIs have many fewer sexual side effects. If you tell some depressed guy that the reason he can't get it up is because of the SSRI he's on, he's not going to give a rat's *** about whether or not he can eat avocados.

 

[asecin]

I've taken several -- imipramine, for a month; Amitriptyline, a couple times to sleep; & desipramine, for about a year (before switching to bupropion xl). I've also taken mirtazapine. What I've posted above was consistent with my experiences. (Also I've contributed significantly to several wikipedia articles on many of these drugs and am active w/ wikiprojectharmacology)

why did you at the end switch to welbutrin ?

 

[pizzystrizzy]

why did you at the end switch to welbutrin ?

Well, I stopped taking the desipramine for a few weeks when I was traveling and forgot to refill it, and I didn't notice much of a difference, so when I came back I decided to try something different. I had been more reticent to try bupropion b/c I was concerned it would weaken the amphetamine sort of along the lines that an SSRI interferes with MDMA, which is why I decided to try desipramine in the first place. So when I started with the bupropion, I got the SR version and took it after the amphetamine had reached maximum concentration. A few months later, I had to teach an 8am class, so I had to wake up at 5 in order to have time to walk my dog and get ready and drive and prepare etc., and I just took everything at once before I left and realized that, contrary to my theory, everything worked a lot better that way. So I decided to switch to xl and continued to do so after my schedule changed again. I'm still not 100% sure exactly what explains my various subjective experiences with the timing of the combination -- I have a few ideas but it is really just speculation.

 

[arctica]

If you haven't tried Wellbutrin XL yet (what have you tried so far?), I would give that a whirl before going to the TCAs. In general, it's very well tolerated, not a lot of side effects, available in generic, and easy to dose (everyone gets a dose of 300mg, more or less). The biggest downside to Wellbutrin that I see is that it doesn't seem as "strong" as other antidepressants. That being said, it's still my favorite (or least hated) antidepressant that I've tried. I find that it's enough to pull me out of a minor depression, but not a major depression by itself. The problem with Wellbutrin XL is that increasing the dosage beyond 300mg (I've tried up to 450mg, now I'm back to 300mg) doesn't seem to increase its effectiveness much, but it does increase the side effects and lowers your seizure threshold. Still, it's definitely one of the better antidepressants out there, and relatively benign.

 

[asecin]

what i know about wellbutrin is that it is mostly a stimulant compared to other antidepressants and its one of the very few that can be abused.

but to what concerns me really is, how come TCAs do not have the same sexual dysfunction problems as SSRIs ? both classes seem to specifically deal with serotonin reuptake inhibition. but TCAs do not show same sexual side effect as SSRIs ?

 

[ebola?]

Because "tricyclic" describes the molecular structure, not the pharmacological activity, they are actually somewhat diverse in action. My guess would be that some have poor affinity for SERT, and some have receptor specific serotonergic antagonism (I'm forgetting at which sites) which counters the sexual dysfunction caused by an excess of serotonin.

ebola

 

[choco1ate]

i was prescribed amitriptyline for sleep and it works well. only side effect so far is the nasty dry mouth, and that just motivates me to drink more water and brush my teeth before going to bed(i used to only do it in the morning). it's definitely "strong" in that the antidepressant effect is immediate
also take wellbutrin xl 150mg. as far as i'm aware this combination is better for my depression than when i took just an ssri or ssri + antipsychotic(bleh)

 

[asecin]

Because "tricyclic" describes the molecular structure, not the pharmacological activity, they are actually somewhat diverse in action. My guess would be that some have poor affinity for SERT, and some have receptor specific serotonergic antagonism (I'm forgetting at which sites) which counters the sexual dysfunction caused by an excess of serotonin.

ebola

why would excess serotonin cause sexual dysfunction anyway ? from what i read before excess serotonin can also cause heart problems and i had that experienced first hand by abusing mdma. kind of sad that serotonin has so many applications throughout the whole body from the guts to the head and if thats evolution, then its pretty crappy one. or if someone believes man was created by higher power, then again, that higher power must be quite moronic

 

[choco1ate]

why would excess serotonin cause sexual dysfunction anyway ? from what i read before excess serotonin can also cause heart problems and i had that experienced first hand by abusing mdma. kind of sad that serotonin has so many applications throughout the whole body from the guts to the head and if thats evolution, then its pretty crappy one. or if someone believes man was created by higher power, then again, that higher power must be quite moronic

i feel a little dumber having read your posts. really, the evolution comment? stop being daft

 

[asecin]

^ ?

ebola?, do you have an idea which serotonin receptor was related to heart problems when taking drugs inhibiting it long term, was it 5-HT2b ?
i was reading how pergolide was withdrawn from usa market because of its heavy toll on 5-HT2b and causing heart valve damage. do you think only this serotonin receptor is to blame for it ? or maybe others have some significant effect ? because when i abused mdma i had heart problems, but mdma doesnt affect 5-HT2b.... so i assume few others do the job too

ugh nevermind, just checked, mdma is agonist at 5-HT2b.

question still stands, are any other serotonin receptors besides this one that affect the heart in a negative way ? it seems even the antagonists cause valve problems which means its double edge sword that receptor, i see a great deal of avoiding affecting it completely.

 

[sekio]

selective 5-ht2B agonism is associated with cardiac valve hyperproliferation. (c.f. fenfluramine, there were class action lawsuits around this). that does not mean that it is acutely cardiotoxic - even select 5ht2b agonists (shulgin's MEM) have been assayed in humans with no apparent ill effects. the real concern is chronic or regular usage.

curiously enough though, SSRIs have not been observed to exhibit the same effect, suggesting that it is only full agonists at this receptor (5ht2b) that are cause for concern, and not an elevated level of postsynaptic serotonin.

 

[Wizzle]

Because "tricyclic" describes the molecular structure, not the pharmacological activity, they are actually somewhat diverse in action. My guess would be that some have poor affinity for SERT, and some have receptor specific serotonergic antagonism (I'm forgetting at which sites) which counters the sexual dysfunction caused by an excess of serotonin.

ebola

Probably true, since clomipramine, which is, I think, the most serotonergic of the TCA's is known to cause libido loss and limp dick. Much moreso then the more noradrenergic ones like nortriptyline.

TCAs are also known to trigger mania, so watch out for that.

 

[arctica]

kind of sad that serotonin has so many applications throughout the whole body from the guts to the head and if thats evolution, then its pretty crappy one.

Maybe we're supposed to be evolved enough at this point to make less sloppy pharmaceutical agents which target a very specific part of the physiological process rather than the shotgun approach that most drugs use. Or, make greater advances in drug delivery. Right now, research disrupting the BBB with focused ultrasound for drug delivery is pretty awesome.

 

[ebola?]

kind of sad that serotonin has so many applications throughout the whole body from the guts to the head and if thats evolution, then its pretty crappy one.

Well, evolutionarily, serotonin is very old (hell, marine invertebrates use it to communicate--barnacles are attracted to the compound), so we would expect it to have been recruited for a diverse array of functions. If anything, this is efficient, as the CNS can regulate serotonergic function in a fine-grained, multifaceted way. It's only really with exogenous ligands that this diversity of function appears as a liability.

ebola

 

[pizzystrizzy]

Well, evolutionarily, serotonin is very old (hell, marine invertebrates use it to communicate--barnacles are attracted to the compound), so we would expect it to have been recruited for a diverse array of functions. If anything, this is efficient, as the CNS can regulate serotonergic function in a fine-grained, multifaceted way. It's only really with exogenous ligands that this diversity of function appears as a liability.

ebola

90% of the human body's serotonin is in the enteric nervous system, the so-called 'second brain.' It's hard to fault evolution for not designing our bodies to be able to consume antidepressants without side effects...

 

[asecin]

selective 5-ht2B agonism is associated with cardiac valve hyperproliferation. (c.f. fenfluramine, there were class action lawsuits around this). that does not mean that it is acutely cardiotoxic - even select 5ht2b agonists (shulgin's MEM) have been assayed in humans with no apparent ill effects. the real concern is chronic or regular usage.

curiously enough though, SSRIs have not been observed to exhibit the same effect, suggesting that it is only full agonists at this receptor (5ht2b) that are cause for concern, and not an elevated level of postsynaptic serotonin.

i was asking ebola? this and expected he will answer instead but ill try to bypass this confusion

what do you think mdma's effect on 5htb2 is ? partial agonist, full agonist, very selective ? because when i took it regularly i developed heart problems. but also i had the very similar effect from certain antidepressants not supposely affecting 5htb2 like effexor. also 5htp dietery supplement had minor signs of it in high enough doses regular use. i believe none of them is really that affective for that specific receptor so i assume some kind of nonselective various subtype of serotonin receptors at play here. just wish i find out which other might be involved in heart problems as to avoid.

 

[ebola?]

i was asking ebola? this and expected he will answer instead but ill try to bypass this confusion

Be glad you're talking to sekio: he gave and will give you better answers than I 'cause he knows more about the topic.

ebola